The investigators' long term goals are to understand and prevent accelerated coronary artery disease following heart transplantation. Findings suggest that abnormal regulation and response to vascular smooth muscle growth factors may be important mechanisms leading to myointimal hyperplasia. Expression of the potent vascular smooth muscle growth factor, heparin binding acidic fibroblast growth factor (aFGF) is rapidly and dramatically increased in human hearts following transplantation, and both the number and functional type of FGF receptors are altered in the transplanted heart. Secreted isoforms of FGF receptor-1 (FGFR1) are present in normal hearts but are increased 30 to 50-fold in allografts. In contrast, transmembrane isoforms of FGFR1, are expressed only in allografts, predominantly during rejection episodes. Thus, events occurring during rejection, including production of IL-6 and TGF-B, modify the normal patterns of alternative MRNA splicing that control local expression of the FGFR1 gene. The investigators hypothesize that immunologic injury within the myocardium and in donor vessels leads to increased production of aFGF and enhanced response to this growth factor via expression of signaling isoforms of its receptor. To test this hypothesis, they will confirm that similar events occur in an inbred rat model of cardiac transplantation that results in vascular disease like human cardiac allograft vasculopathy (CAV); using the rat model, they will inhibit FGFR1 dependent signals by in-vivo transfection of an aFGF inhibitor and assess its efficacy in preventing the development of CAV. To facilitate the ultimate use of in vivo transfection in clinical transplantation, they will prospectively correlate the development of coronary intimal thickening in human cardiac allografts with expression of aFGF and isoforms of its receptors.